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Application of heme oxygenase-1, carbon monoxide and biliverdin for the prevention of intestinal ischemia/reperfusion injury.

Nakao A, Kaczorowski DJ, Sugimoto R, Billiar TR, McCurry KR - J Clin Biochem Nutr (2008)

Bottom Line: Intestinal ischemia/reperfusion (I/R) injury occurs frequently in a variety of clinical settings, including mesenteric artery occlusion, abdominal aneurism surgery, trauma, shock, and small intestinal transplantation, and is associated with substantial morbidity and mortality.Although the exact mechanisms involved in the pathogenesis of intestinal I/R injury have not been fully elucidated, it is generally believed that polymorphonuclear neutrophils, pro-inflammatory cytokines, and mediators generated in the setting of oxidative stress, such as reactive oxygen species (ROS), play important roles.Heme oxygenase (HO) is the rate-limiting enzyme that catalyzes the degradation of heme into equimolar quantities of biliverdin and carbon monoxide (CO), while the central iron is released.

View Article: PubMed Central - PubMed

Affiliation: Thomas E. Starzl Transplantation Institute, Department of Surgery, University of Pittsburgh Medical Center, Pittsburgh, PA 15213, USA.

ABSTRACT
Intestinal ischemia/reperfusion (I/R) injury occurs frequently in a variety of clinical settings, including mesenteric artery occlusion, abdominal aneurism surgery, trauma, shock, and small intestinal transplantation, and is associated with substantial morbidity and mortality. Although the exact mechanisms involved in the pathogenesis of intestinal I/R injury have not been fully elucidated, it is generally believed that polymorphonuclear neutrophils, pro-inflammatory cytokines, and mediators generated in the setting of oxidative stress, such as reactive oxygen species (ROS), play important roles. Heme oxygenase (HO) is the rate-limiting enzyme that catalyzes the degradation of heme into equimolar quantities of biliverdin and carbon monoxide (CO), while the central iron is released. An inducible form of HO (HO-1), biliverdin, and CO, have been shown to possess generalized endogenous anti-inflammatory activities and provide protection against intestinal I/R injury. Further, recent observations have demonstrated that exogenous HO-1 expression, as well as exogenously administered CO and biliverdin, have potent cytoprotective effects on intestinal I/R injury as well. Here, we summarize the currently available data regarding the role of the HO system in the prevention intestinal I/R injury.

No MeSH data available.


Related in: MedlinePlus

Heme Oxygenase System
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Related In: Results  -  Collection


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Figure 1: Heme Oxygenase System

Mentions: Initially, HO was recognized as the enzyme responsible for heme catabolism by opening its tetrapyrrole ring structure to yield CO, biliverdin, and free iron [5]. Biliverdin is rapidly reduced to bilirubin by biliverdin reductase (Fig. 1). Since inducible HO-1 was discovered and found to be a stress-responsive protein with broad cytoprotective properties, interest in the HO system has been renewed and it has attracted the attention of the scientific community worldwide [8, 9].


Application of heme oxygenase-1, carbon monoxide and biliverdin for the prevention of intestinal ischemia/reperfusion injury.

Nakao A, Kaczorowski DJ, Sugimoto R, Billiar TR, McCurry KR - J Clin Biochem Nutr (2008)

Heme Oxygenase System
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2266059&req=5

Figure 1: Heme Oxygenase System
Mentions: Initially, HO was recognized as the enzyme responsible for heme catabolism by opening its tetrapyrrole ring structure to yield CO, biliverdin, and free iron [5]. Biliverdin is rapidly reduced to bilirubin by biliverdin reductase (Fig. 1). Since inducible HO-1 was discovered and found to be a stress-responsive protein with broad cytoprotective properties, interest in the HO system has been renewed and it has attracted the attention of the scientific community worldwide [8, 9].

Bottom Line: Intestinal ischemia/reperfusion (I/R) injury occurs frequently in a variety of clinical settings, including mesenteric artery occlusion, abdominal aneurism surgery, trauma, shock, and small intestinal transplantation, and is associated with substantial morbidity and mortality.Although the exact mechanisms involved in the pathogenesis of intestinal I/R injury have not been fully elucidated, it is generally believed that polymorphonuclear neutrophils, pro-inflammatory cytokines, and mediators generated in the setting of oxidative stress, such as reactive oxygen species (ROS), play important roles.Heme oxygenase (HO) is the rate-limiting enzyme that catalyzes the degradation of heme into equimolar quantities of biliverdin and carbon monoxide (CO), while the central iron is released.

View Article: PubMed Central - PubMed

Affiliation: Thomas E. Starzl Transplantation Institute, Department of Surgery, University of Pittsburgh Medical Center, Pittsburgh, PA 15213, USA.

ABSTRACT
Intestinal ischemia/reperfusion (I/R) injury occurs frequently in a variety of clinical settings, including mesenteric artery occlusion, abdominal aneurism surgery, trauma, shock, and small intestinal transplantation, and is associated with substantial morbidity and mortality. Although the exact mechanisms involved in the pathogenesis of intestinal I/R injury have not been fully elucidated, it is generally believed that polymorphonuclear neutrophils, pro-inflammatory cytokines, and mediators generated in the setting of oxidative stress, such as reactive oxygen species (ROS), play important roles. Heme oxygenase (HO) is the rate-limiting enzyme that catalyzes the degradation of heme into equimolar quantities of biliverdin and carbon monoxide (CO), while the central iron is released. An inducible form of HO (HO-1), biliverdin, and CO, have been shown to possess generalized endogenous anti-inflammatory activities and provide protection against intestinal I/R injury. Further, recent observations have demonstrated that exogenous HO-1 expression, as well as exogenously administered CO and biliverdin, have potent cytoprotective effects on intestinal I/R injury as well. Here, we summarize the currently available data regarding the role of the HO system in the prevention intestinal I/R injury.

No MeSH data available.


Related in: MedlinePlus